Indap capsules 2.5mg №10×3

Name:
Indap.
Description:
The main active ingredient is indapamide. Release formCapsules. Dosage 2.5 mg. Preclinical data on the safety of the drug The results of experimental toxicological studies of indapamide are very favorable. Only megadoses cause signs of acute toxicity, the lethal dose is 300-1000 mg/kg bw, subacute toxicity after oral administration for three months was observed in laboratory rats at a dose of 1000 mg, chronic toxicity at a dose of 30 mg is due to hypokalemia. Testing for mutagenicity, carcinogenicity, reproductive toxicity gave negative results. Pharmacological group Diuretics. Sulfonamides. ATC code: C03BA11. Pharmacodynamics Indapamide is a derivative of non-thiazide sulfonamides, with an indole ring, it is pharmacologically similar to thiazide diuretics, which act by inhibiting sodium reabsorption in the cortical segment of the distal tubule of the nephron. Indapamide increases the excretion of sodium and chlorides in the urine, and to a lesser extent the excretion of potassium and magnesium, thereby increasing the volume of urine formation; the drug has an antihypertensive effect. The antihypertensive effect persists in anephritic hypertensive patients. Like other diuretics, the vascular mechanism of action of indapamide includes: Decrease in the tone of the smooth muscles of the walls of blood vessels associated with transmembrane exchange of ions (primarily calcium). Stimulation of the synthesis of prostaglandin PGE2 and prostacyclin PGI2 (vasodilator and inhibitor of platelet aggregation). Indapamide reduces left ventricular hypertrophy. In thiazide and similar diuretics, the therapeutic effect, starting from a certain dose, no longer increases, and the manifestations of side effects increase. Therefore, in case of treatment failure, it is not recommended to increase the dose. Indapamide does not affect the level of LDL and HDL cholesterol and blood glucose. PharmacokineticsAbsorption The bioavailability of indapamide is very high (93%). The time required to reach the maximum serum concentration (Tmax) ranges from 1-2 hours after taking a dose of 2.5 mg. Distribution More than 75% of indapamide binds to plasma proteins. The elimination half-life is 14-24 hours (average 18 hours). Repeated administration of indapamide increases steady state plasma concentrations compared with a single dose. Steady state remains stable, no cumulative effect is observed. Metabolism 60-80% of the dose taken is excreted by the kidneys. Basically, indapamide is excreted in the form of metabolites, 5% is excreted in unchanged form. In renal failure, pharmacokinetic parameters do not change. Indications for use Arterial hypertension. Dosage and administration Assign 2.5 mg (1 capsule) per day, in the morning, regardless of food intake. Capsules are swallowed without biting and washed down with water. The drug can be used in combination with other antihypertensive agents, with the exception of diuretics. If the treatment is not effective enough, the dose of Indap should not be increased, it is better to start taking an additional antihypertensive agent. When using higher doses of indipamide, there is no increase in the antihypertensive effect, only its saluretic effect increases. Use during pregnancy and lactation During pregnancy, diuretics are usually not prescribed to women. In no case should the drug be used to treat physiological edema during pregnancy. Diuretics can cause fetoplacental ischemia, which poses a threat to fetal growth. Indapamide passes into breast milk, therefore, during the period of taking the drug, breastfeeding should be stopped. Influence on the ability to drive vehicles and other mechanisms Usually, INDAP® does not affect the level of attention. However, in some cases, especially at the beginning of treatment or when combined with other antihypertensive drugs, due to a decrease in blood pressure, the level of attention may decrease, which will negatively affect the ability to drive vehicles and control mechanisms. Precautions In case of impaired liver function, thiazide diuretics can cause hepatic encephalopathy. In this case, the use of diuretics should be stopped immediately. Plasma sodium level: Plasma sodium concentration should be determined before starting treatment and monitored for changes at regular intervals. Treatment with diuretics may be accompanied by hyponatremia, sometimes with very serious consequences, while in the initial stage, a decrease in the concentration of sodium in the blood may be asymptomatic. Therefore, it is recommended to regularly monitor plasma sodium levels, especially in elderly patients and those suffering from cirrhosis of the liver. Plasma potassium level: Long-term use of thiazide and similar diuretics is associated with a risk of a decrease in plasma potassium concentration and the development of hypokalemia. The occurrence of hypokalemia in patients must be prevented. This is especially true for the elderly, patients suffering from malnutrition, as well as patients taking other drugs simultaneously with a diuretic drug, patients suffering from cirrhotic ascites with edema, as well as patients with coronary vascular disease and heart dysfunction, who are predisposed to the occurrence of arrhythmia ( hypokalemia increases the toxic effect of digitalis preparations on the heart). An increased risk of hypokalemia is also characteristic of patients with an extended QT interval, regardless of the genesis of this phenomenon, which can be congenital or iatrogenic. Hypokalemia, as well as bradycardia, in this case predisposes to the occurrence of severe arrhythmias, including deadly ventricular tachycardia (torsades de pointes). In all these cases, it is necessary to more often monitor the concentration of potassium in the plasma. An examination to detect possible hypokalemia should be carried out in the first week of treatment. If signs of hypokalemia are detected, appropriate measures should be taken to prevent it. Plasma calcium levels: Thiazide and similar diuretics may decrease urinary calcium excretion, which may lead to a slight and transient increase in plasma calcium concentration. Hypercalcemia may be the result of previously undiagnosed hyperparathyroidism. In this case, treatment should be stopped and an examination of the function of the parathyroid glands should be carried out. Blood glucose level: In patients with diabetes, especially in the presence of hypokalemia, it is necessary to regularly monitor the level of glucose in the blood. Uric acid level: Patients with elevated uric acid levels may experience gout attacks, so the dose of the drug should be adjusted depending on the current levels of its level in plasma. Thiazide and thiazide-like diuretics are most effective only with normal or minimally reduced kidney function (plasma creatinine level less than 25 mg / l, that is, 220 micromol / l in adults). Hypovolaemia due to loss of water and sodium during treatment with diuretics reduces glomerular filtration, which is sometimes accompanied by an increase in plasma urea and creatinine. In patients with normal renal function, this temporary functional renal failure usually does not lead to serious consequences, however, its occurrence can significantly exacerbate already existing renal failure. Indapamide may cause a positive reaction in doping tests. The preparation contains lactose. Patients with a rare hereditary disease of galactose intolerance, Lapp lactase deficiency or malabsorption of glucose and galactose are not recommended to use this drug. Interaction with other drugs Undesirable combinations: The simultaneous use of indapamide with lithium can lead to an increase in the level of lithium in the blood plasma with signs of an overdose, for example, with a salt-free diet (reduced urinary excretion of lithium). If the use of diuretics is necessary, then the plasma lithium level should be systematically monitored and the dose adjusted accordingly. Some drugs (astemizole, bepridil, erythromycin, halofantrine, sultopride, terfenadine, vincamine), taken together with indapamide, in patients suffering from hypokalemia, bradycardia or with a prolonged QT interval, can cause ventricular tachycardia (torsades de pointes). Combinations requiring increased caution: Non-steroidal antirheumatic drugs used systemically and high doses of salicylates may reduce the antihypertensive effect of indapamide. Dehydrated patients are at risk of acute renal failure (reduced glomerular filtration). Therefore, at the beginning of treatment, the patient with systematic monitoring of kidney function should drink plenty of water. Amphotericin B Amphotericin B (iv), glucocorticoids and mineralocorticoids used systemically, tetracosactide, contact laxatives can cause hypokalemia (the effect is cumulative). It is necessary to monitor the levels of potassium in the blood plasma and, if necessary, correct them, especially with simultaneous treatment with digoxin. Baclofen increases the antihypertensive effect. At the beginning of treatment, the patient with systematic monitoring of kidney function should drink plenty of water. In patients using digoxin, existing hypokalemia may increase the risk of toxic effects of digoxin. In these cases, you should systematically monitor the level of potassium in the plasma, record the ECG, and, if necessary, change the treatment. Angiotensin-converting enzyme (ACE) inhibitors at the beginning of treatment and with simultaneous sodium deficiency (especially in patients with renal artery stenosis) increase the risk of sudden hypotension or acute renal failure. In essential hypertension, when previous diuretic therapy may have caused sodium deficiency, it is recommended to stop taking diuretics three days before starting treatment with an ACE inhibitor. In chronic heart failure, in the case of combining indapamide with an ACE inhibitor, it is necessary to start treatment with a very low dose of an ACE inhibitor and a low dose of a diuretic. In this case, during the first weeks of treatment with an ACE inhibitor, it is necessary to systematically monitor kidney function (plasma creatinine levels). While taking antiarrhythmic drugs of class Ia (quinidine, disopyramide) and class III (amiodarone, bretylium, sotalol), it is necessary to take into account the risk of ventricular tachycardia (hypokalemia, bradycardia and already existing extended QT interval are predisposing factors). When taking metformin, there is a risk of lactic acidosis associated with possible insufficiency of kidney function due to the intake of diuretics (most often loop diuretics). It is recommended not to prescribe metformin if plasma creatinine levels exceed 15 mg/l (135 micromol/l) in men and 12 mg/l (110 micromol/l) in women. High doses of iodine-containing contrast agents in combination with indapamide and with simultaneous dehydration increase the risk of acute kidney failure. Imipramine (tricyclic) antidepressants and antipsychotics increase the antihypertensive effect and increase the risk of orthostatic hypotension (the effect is cumulative). When taking calcium salts, there is a risk of hypercalcemia as a result of a decrease in calcium excretion in the urine. Cyclosporine leads to the risk of increasing plasma creatinine levels without changing the level of circulating cyclosporine (even without reducing the water/sodium ratio). Corticosteroids, as a result of sodium and water retention, may reduce the antihypertensive effect. Appointment with potassium-sparing diuretics (amiloride, spironolactone, triamterene) is a rational combination, very useful for some patients, does not exclude the possibility of hypokalemia, and in patients with kidney dysfunction or diabetes, hyperkalemia. In these cases, the level of potassium in the plasma should be monitored, if necessary, an ECG, if necessary, change the treatment. Contraindications severe forms of renal failure severe forms of liver failure (including hepatic encephalopathy) hypokalemia hypersensitivity to sulfonamide derivatives or excipients of the drug for children under 18 years of age pregnancy and lactation. Composition 1 capsule contains 2.50 mg of indapamide (indapamidum) Excipients: granulated microcrystalline cellulose, lactose monohydrate, corn starch, magnesium stearate, colloidal silicon dioxide; composition of the gelatin capsule: gelatin, indigo carmine, titanium dioxide. Overdose Indapamide was found to have no toxic effect up to a dose of 40 mg, i.e. 16 times the therapeutic dose. Signs of acute poisoning are symptoms of hypovelemia (hyponatremia, hypokalemia). Nausea, vomiting, hypotension, convulsions, dizziness, drowsiness, states of confusion and confusion, polyuria or oliguria, and even anuria (as a result of hypovolemia) may be observed. Treatment: gastric lavage, correction of water and electrolyte balance, symptomatic therapy. There is no specific antidote. Side effects Most of the side effects that affect clinical and laboratory parameters are dose dependent. In some cases, nausea, constipation, dry mouth, dizziness, fatigue, paresthesia, headaches may occur. As a rule, adverse reactions are weakened with a decrease in dose. Very rarely, pancreatitis can occur. In persons predisposed to allergic and asthmatic reactions, hypersensitivity reactions, especially dermatological ones, may occur. In the case of already existing acute disseminated lupus erythematosus, there is a danger of deterioration, the appearance of a maculopapular rash on the skin, purpura. Liver failure may cause encephalopathy (see Contraindications Special Warnings and Precautions for Use). In addition, indapamide can cause laboratory changes in the form of potassium deficiency leading to hypokalemia, especially in risk groups (see section Special warnings and precautions for use), and can also cause hyponatremia with hypovolemia, leading to dehydration and orthostatic hypotension. In clinical studies, when taking a therapeutic dose after treatment lasting 4-6 weeks, cases of hypokalemia were noted (plasma potassium levels do not exceed 3.4 mmol / l in 25% of patients and less than 3.2% mmol / l in 10% of patients) . After treatment lasting 12 weeks, the average decrease in plasma potassium levels reached a value of 0.41 mmol/l. Simultaneous loss of chloride ions can cause secondary metabolic alkalosis. The probability of occurrence and intensity of manifestation of this effect is low. It is necessary to carefully weigh the indications for the appointment of this diuretic drug in patients with gout or diabetes, if they experience an increase in the level of uric acid and blood sugar during the period of treatment. In some cases, hematological diseases (thrombocytopenia, leukopenia, aplastic anemia, hemolytic anemia) may occur. In exceptional cases, hypercalcemia may develop. Storage conditions Store in a dry, dark place at a temperature not exceeding 25 °C. Keep away from children. Buy Indap capsules 2.5 mg No. 10×3 Price for Indap capsules 2.5 mg No. 10×3 Instructions for use for Indap capsules 2.5 mg No. 10×3